PPARγ agonist inhibits high glucose-induced production of reactive oxygen species by UCP2 up-regulation |
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| Authors: | WANG Pei-jian WANG Qiu-lin YANG Zhen WANG Fang PU Chun-hua LI Wen-zhang LIANG Deng-pan ZHOU Peng |
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| Institution: | Department of Cardiology, The First Affiliated Hospital, Chengdu Medical College, Chengdu 610500, China |
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| Abstract: | AIM: To explore the effects of PPARγ on the elevated level of reactive oxygen species (ROS) induced by high glucose and its mechanism. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured with DMEM containing high glucose (33 mmol/L D-glucose), and DMEM containing lower glucose (5.5 mmol/L D-glucose) was used as control. Superoxide anion and nitric oxide fluorescence probes were used to observe the effects of PPARγ agonist on ROS and NO productions in the HUVECs. The uncoupling protein 2 (UCP2) protein level in the HUVECs was detected by Western blotting. RESULTS: PPARγ agonist pioglitazone inhibited the ROS generation and prevented the decrease in NO level under high glucose condition, and these effects were reversed by pretreatment with PPARγ antagonist GW9662. The results of Western blotting indicated that PPARγ agonist pioglitazone up-regulated the UCP2 expression under high glucose condition, and this effect was also blocked by GW9662. Inhibition of UCP2 by genipin attenuated the effect of pioglotazone on the ROS production. CONCLUSION: Activation of PPARγ inhibits ROS generation under high glucose condition, and this effect may mediate by up-regulation of UCP2. |
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| Keywords: | Peroxisome proliferator-activated receptor γ Uncoupling protein 2 Oxidative stress Endothelial cells |
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